obstetric revision article internacional colaboration ... · obstetric revision article...

Obstetric

Revision articleInternacional colaboration

Fetal MRI: thoracic, abdominal and pelvic pathologyManuel Recio Rodríguez (1), Pilar Martínez Ten (2), Javier Pérez Pedregosa (2),Carmina Bermejo López (3), Inés Tamarit Degenhardt (4), Ignacio Pastor Abascal (1).

ResumenAunque la ecografía (US) es el método de elección enla evaluación del feto, la resonancia magnética (RM) esuna técnica complementaria a la US en el diagnósticode las anomalías fetales. Entre las ventajas de la RM sedestacan un excelente contraste tisular, un campo devisión grande y una relativa operador-independencia.La mayoría de los trabajos previos de RM fetal hanestudiado el sistema nervioso central (SNC). Sinembargo, la RM es útil en la evaluación de las anoma-lías torácicas y abdominales. En este artículo se mues-tran los diferentes aspectos por RM de las anomalíasfetales torácicas y abdominales y se discuten las indi-caciones y ventajas de la RM fetal.Palabras clave. Anomalías fetales. Ecografía fetal.Estudios comparativos, resonancia magnética (RM).RM embarazo. RM fetal.

AbstractFetal MRI: thoracic, abdominal and pelvic pathology.Ultrasonography (US) is the method of choice in fetal exam-ination. However, magnetic resonance (MR) imaging is acomplementary technique that contributes to the accuratediagnosis of fetal anomalies. The benefits of MR includeexcellent tissue contrast, large field of view and relative oper-ator independence. Most previous reports on fetal MR havefocused on central nervous system (CNS). However, MR is auseful tool for the examination of fetal thoracic and abdomi-nal anomalies. This article illustrates the different features offetal thoracic and abdominal anomalies on MR, and furtherdiscusses the indications and benefits of fetal MR.Keywords. Comparative studies. Fetal anomalies. FetalMR. Fetal US. Magnetic resonance (MR) imaging.Pregnancy MR. Rapid imaging.

INTRODUCTION

Ultrasound (US) is the routine screening test forfetal anomalies but, even when performed by expe-rienced personnel, it has technical limitations. Even ifmost ultrasound examinations are diagnostic, suchlimitations may require an alternative imagingmethod in more complex cases to confirm or comple-te ultrasound findings, to guide management of preg-nancy and to plan intrauterine interventions, delivery,and postnatal care.

With the advent of ultrafast sequences in the1990’s, magnetic resonance imaging (MRI) is beco-ming a non-invasive method complementary to ultra-sound, useful in the detection of fetal anomalies,which is helpful in formulating prognosis and perina-tal management. However, most published researchhas focused on brain pathology and only a few studiesreport the use of fetal MRI in thoracic, gastrointestinalor genitourinary abnormalities. This article reviewsfetal thoracic anomalies (with an especial emphasis oncongenital diaphragmatic hernia, where MRI playsthe most important role) and describes the main indi-cations for MRI in abdominal pathology, as well as theadvantages and disadvantages of MRI as compared toultrasound.

IMAGING PROTOCOL

Scans should be performed using high-field (1.5T)resonators with multi-channel coils of great spatialresolution. Three orthogonal planes with respect tothe mother are identified to obtain sagittal, coronaland axial slices of the fetus, always taking as referen-ce the last sequence used to plan the followingsequence because of fetal movements. The mainsequences used are (Fig. 1):• T2-weighted images --such as Single Shot Fast Spin

Echo T2 (SSFSE T2)-- )-- and balanced Steady-StateFree Precession sequences—such as FIESTAsequence, with high tissue contrast, showing hype-rintense amniotic fluid. Both sequences are usefulto study the airways, lung, urinary tract and gas-trointestinal tract—from the esophagus to the loopsof the proximal ileum. All these structures are hype-rintense on T2-weighted images. The FIESTAsequence is also useful in assessing vascular ana-tomy without intravenous contrast, showing hype-rintense fetal vessels (vessels appear hypointenseon SSFSE T2- and T1-weighted images).

• T1-weighted images (3D gradient dual echo, 2DFSPGR or 3D LAVA): provide less tissue contrastthan SS FSE T2 or FIESTA. They are useful in the

(1) Hospital Universitario Quirón- Madrid, España.C/Diego de Velázquez 1, Pozuelo de Alarcón (28223)- Madrid, España.(2) Delta Ecografía. Centro de Diagnóstico por la Imagen en Obstetriciay Ginecología, Madrid. (3) Gabinete Médico Velázquez. Madrid.

(4) Servicio de Ginecología y Obstetricia. Hospital La Moraleja. Madrid.Correspondencia: Dr. Recio Rodríguez- [email protected]: agosto 2011; aceptado: diciembre 2011Received: august 2011; accepted: december 2011©SAR

RAR - Volumen 76 - Número 1 - 2012 Página 1

Fetal MRI: thoracic, abdominal and pelvic pathology

assessment of the liver, the loops of the distalileum and colon, which are visualized as hyperin-tense structures. 3D sequences offer the possibilityof volume reconstructions of the entire colon. Asin brain pathology, these sequences are useful todetermine the presence of subacute bleeding, cal-cifications or lipomas (1).

• Diffusion-weighted imaging: its applications areevolving and it is currently being used in theassessment of lung parenchyma maturation (2) andin the study of renal pathology, such as renalvenous thrombosis or the Twin-Twin TransfusionSyndrome (TTTS) (3).

THORACIC PATHOLOGY

Fetal lungs are filled with fluid, and are thereforehyperintense on T2-weighted imaging, easily diffe-rentiated from other organs. MRI will not replace USas a first-line screening technique, but is useful incases of oligohydramnios, maternal obesity, and unfa-vorable fetal position. Levine et al. (4) examined by US74 fetuses diagnosed with thoracic abnormalities. MRIyielded additional information in 38% of cases andaffected care in 8%.

Congenital diaphragmatic hernia

Congenital diaphragmatic hernia (CDH) is themain indication for fetal MRI in thoracic pathology.The incidence of CDH is 1 in 2,500 to1 in 5,000 livebirths (5), with 85% occurring on the left side(Bochdalek hernia), 15% on the right and 2% are bila-teral (6). Approximately 40% of patients with CDHhave other congenital malformations (mainly cardiacand of the central nervous system –CNS-), chromoso-mal anomalies (trisomy 21, trisomy 18 and trisomy 13)and genetic syndromes (Fryns syndrome, Langesyndrome or Marfan syndrome) (7). Associated anoma-lies are considered an independent survival factor(survival is less than 15%) (8).

The degree of pulmonary hypoplasia and liverherniation are the main prognostic factors. To calcula-te lung volume on ultrasound, the lung-to-head ratio(LHR) (contralateral lung area / head circumference)is used, and it is measured in the second trimester. IfLHR is >1.6, survival is ≥83%; if LHR is ≥ 1 and < 1.6,survival is 66%; and with values ≥0.8 and <1, survivalis 16% (9). Volumetric evaluation of the lung using 3Dultrasound for calculation of lung volume is not betterthan LHR (10).

With MRI, both the ipsilateral and contralaterallung volumes can be measured, thus obtaining theobserved total fetal lung volume (TFLV).

Rypens et al (11) conducted a multicenter (sevenhospitals in France and Belgium) prospective studywith MRI in 336 fetuses suspected of having CNS

disorders, to establish the correlation between totallung volume and gestational age. Predicted or expec-ted lung volume (ELV) is calculated by the equation:ELV = 0.0033g2.86 (where g is gestational age inweeks).

In their retrospective study of 46 fetuses fromAmerican women, Coakley et al (12) found a strongcorrelation between total lung volume measured atMRI and liver volume measured at MRI, fetal weightestimated at US, head circumference measured at USand gestational age. The ELV is calculated by theequation: ELV = (0.47 ≥ liver volume in milliliters) +(0.76 ≥ biparietal diameter in millimeters) ≥ (0.39 ?femur length in millimeters) ≥ 18.9.

In addition, Cannie et al. (13) conducted a study in200 fetuses without abnormalities at UniversityHospital Gasthuisberg (Belgium). Total lung volumecorrelated best with fetal body volume (FBV) thanwith all other biometric variables. The ELV is calcula-ted by the equation: ELV = (2.0 x 10-9 x FBV3) – (1.19x 10 -5 x FBV2) + (0.0508 x FBV) – 1.79.

The observed-expected (O/E) ratio for TFLV x 100establishes the relative lung volume (RLV) and valuesbelow 80% are considered as hypoplasia (14). All fetu-ses with values < 14.3% have a 100% mortality rate,those with values >32.8 have a 100% survival rate andthose with values >44% do not need extracorporealmembrane oxygenation (ECMO) (15) (Figs. 2, 3 and 4).

MRI is also useful in the assessment of lung matu-ration by lung signal intensity: lung maturation hasbeen correlated with a high signal intensity of thelung on T2-weighted images, calculating signal inten-sity ratios of lung/spinal fluid (16), lung/gastric fluidor lung/liver (17). Signal intensity increases with gesta-tional age (18).

Moore et al (19) have studied fetal lungs using diffu-sion-weighted imaging and have shown that the ADCincreases with gestational age (as from week 18), pro-bably reflecting the increase in alveolar fluid secretionand pulmonary vascularization (20,21).

Spectroscopy has theoretical potential for evalua-tion of lung maturation. Surfactant is composed of90% phospholipids (basically 70% phosphatidylcholi-ne—lecithin) and 10% protein. The amount of choline,the ratio of choline/creatine, lecithin and lactatemight be correlated with the amount of pulmonarysurfactant (22,23). Unfortunately, this technique has seve-ral limitations (especially fetal motion artifacts).

Fetuses with liver herniation have 50% survival.The supradiaphragmatic liver position is difficult tovisualize on US, while MRI allows identification ofdiaphragmatic defect (defect in the low-signal-inten-sity band on T2-weighted sequences), especially insagittal and coronal planes, and the abnormal positionof the liver (with hyperintense signal on T1-weightedimages and hypointense signal on T2-weightes ima-ges). The most commonly herniated structures in left-sided diaphragmatic hernias include omental fat, thesmall bowel, the left hepatic lobe and the stomach.

Página 2 RAR - Volumen 76 - Número 1 - 2012

Manuel Recio Rodríguez et al.

The kidney and pancreas are rarely herniated. Inright-sided diaphragmatic hernias, the most com-monly herniated organ is the liver with herniation ofthe right hepatic lobe.

Fetal endoluminal tracheal occlusion (FETO) isindicated for liver herniation (LHR <1, at week 26-29and in the absence of chromosomal anomalies or asso-ciated abnormalities). FETO is a minimally invasiveprocedure in which an endotracheal balloon is infla-ted for 3 or 6 weeks. Retention of fluid within the lungaccelerates lung maturation and reduces the risk ofpulmonary hypertension. FETO should be performedprior to 29 weeks of gestation, and the balloon is thenremoved via fetoscopy --after being punctured atweek 34-- either by ex-utero intrapartum treatment(EXIT) or post-natal (either by tracheoscopy or percu-taneous puncture). When FETO is performed before29 weeks of gestation, a significant lung expansionoccurs as a result of a marked production of fluids.When the balloon is removed, the RLV decreases bynearly 50%, but it is 40% higher than the RLV prior toballoon insertion. When FETO is performed after 29weeks of gestation, the RLV does not increase afterballoon removal (24).

In the study conducted by Jani et al the main com-plications were: prelabor rupture of membrane (47%),chorioamnionitis and premature delivery. FETO incre-ased survival in left-sided CDH from 24.1% to 49.1%

and in right-sided CDH from 0% to 35.3%. Ninety-seven per cent of fetuses undergoing FETO were liveborn and 50% of those babies resisted surgery andwere discharged from the hospital alive.

Cystic adenomatoid malformation (CAM) or congenital pulmonary airway malformation

CAM is the most commonly diagnosed fetal lungmass of the newborn period. It consists of lung hamar-toma with proliferation of terminal bronchioles andlack of normal alveoli. They are solid or cystic masses,vascularized by the pulmonary artery and with drai-nage via the pulmonary veins. Most CAMs are unila-teral and affect one entire lung lobe, although thereare hybrid lesions associated with pulmonary seques-tration with systemic vascularization (26,27). Stocker et al(28) classified them as: type I (one or more cysts > 2 cm),type II (multiple cysts 2-0.5 cm) and type III (largemicrocystic lesion <0.5 cm). CAMs are usually detec-ted by ultrasound at 20 weeks of gestation (29) and theyappear as cystic or solid echogenic lung masses. Theymay be occasionally misdiagnosed on ultrasound asCDH or vice versa (30).

Isolated CAMs are associated with a good progno-sis, with 97% survival (independent of histologicaltype), excluding CAMs with associated abnormalities,


Fig. 1: (a) Sagittal SSFSE T2. (b) Coronal FIESTA. (c) SS FSE T2 (URO-MRI). (d) diffusion-weighted imaging. (e) Sagittal 3D T1-weighted gra-dient echo. (f) Volume reconstruction (VR) of the colon with 3D LAVA.



Fig. 2: (a), (b) and (c) Sagittal SS FSE T2. (d) Axial SS FSE. (e) VR of the right lung (5.311 cm3) and (f) VR of the left lung (1.425 cm3). Left-sided diaphragmatic hernia with herniated bowel loops (white arrow), stomach (white arrowhead) and left hepatic lobe (curved arrow). Right lung(broken arrow). Heart (black arrowhead). Hypoplasia of the left lung (black arrow) and contralateral cardiomediastinal shift. Expected total fetallung volume: 18.2 cc; observed total fetal lung volume: 6.73 cc; relative lung volume: 36.9%. Gestational Age (GA): 20 weeks.

Fig. 3: (a) Coronal FIESTA and (b) Coronal T1-weighted dual echo gradient. (c) and (d) SagittalSS FSE T2. Right-sided diaphragmatic herniawith herniated bowel loops (black arrow) andright hepatic lobe (white arrow). Hypoplasia ofright lung (arrowhead). Contralateral cardio-mediastinal shift. GA: 22.5 weeks. Right lungvolume: 0.884 cc; left lung volume: 5.905 cc;observed total lung volume: 6.79 cc; expectedtotal lung volume: 20.32 cc; relative lung volu-me: 33%.



Fig.4: (a) Sagittal SS FSE T2, (b) Sagittal T1-weighted dual echo gradient and (c) Coronal SSFSE T2. Left-sided diaphragmatic hernia with par-tially herniated stomach (black arrow), bowel loops (broken arrow), colon’s splenic flexure (curved arrow) and spleen (white arrowhead). Left lung(white arrow). Contralateral cardiomediastinal shift. GA: 21 weeks. Right lung volume: 6.077 cc; left lung volume: 3.063 cc; observed total lungvolume: 9.14 cc; expected total lung volume: 19.2 cc; relative lung volume: 48.05%.

which account for 3-12% (most of them correspondingto Stocker type II lesions). In over 50%, there is spon-taneous resolution during pregnancy (29). Typically,CAMs with less than 57% of total lung volume regresscompletely, while those with a volume greater than84% show partial regression.

The most important prognostic factor is the presen-ce or absence of hydrops (31). CAM may cause compres-sion of the heart and the inferior vena cava and, secon-darily, impair cardiac contractility and venous return(32). If hydrops is left untreated, over 90% of fetuses willdie before being born (33). To estimate the risk of deve-loping hydrops, the CAM volume / head circumferen-ce ratio (CVR) is calculated at ultrasound. CAM volu-me is calculated based on ultrasound measurementsobtained in three dimensions of the mass. The CAMvolume is divided by the head circumference, which isassessed by ultrasound (occipital frontal diameter +biparietal diameter) x 1.57. If the CVR is > 1.6, the fetuswill develop hydrops in 75% of cases; if the CVR is<1.6, hydrops will occur in less than 3% of cases (35).

MRI findings vary according to the type of CAM:type I lesions manifest as hyperintense unilocularlesions on T2-weighted images; type II lesions appearas hyperintense multilocular lesions on T2-weightedimages; type III lesions manifest as hyperintense solidmasses with normal adjacent lung, which is more

hypointense, on T2-weighted images. In addition, thevolume of lesions and lung parenchyma can be calcu-lated, thus allowing quantification and monitoring ofthe lesions growth or resolution (31) (Figs. 5 and 6).

CAMs require postnatal surgery, after one monthof life, because of the risk of infection and the low riskof malignant transformation --annual rate of 3%-- intopleuropulmonary blastoma, rhabdomyosarcoma ormyxosarcoma in infants and into bronchoalveolar car-cinoma in children and adults (36).

Bronchopulmonary sequestration

Bronchopulmonary sequestration is the secondmost common lesion in prenatal diagnosis.Bronchopulmonary tissue is disconnected from thebronchial tree and pulmonary arteries and receivesarterial blood from the systemic circulation, via thethoracic or abdominal aorta. The most common loca-tion is the left lower lobe (>2/3) (37), with 90% beingsupradiaphragmatic (Fig. 7) and less than 10% infra-diaphragmatic (38) (Fig. 8).

Extralobar sequestration occurs in the fetus, has itsown pleural covering and venous drainage is throughthe azygos system or the inferior vena cava (in 25% ofcases through the pulmonary veins) (39). Intralobar



Fig. 5 (a) Coronal SS FSE T2. (b) Sagittal SS FSE T2. (c) Axial SS FSE T2, (d) VR reconstruction of CAM (e) VR reconstruction of the right lung, (f) VRreconstruction of the left lung. CAM type II in lower left lobe (curved arrow), upper left lobe (arrowhead) and right lung (white arrow). GA: 22.5 weeks.Right lung volume: 9.307 cc; left lung volume: 4.244 cc; total lung volume: 13.55 cc. CAM volume: 13.942 cc. CVR index: 0.75 (<1.6 good prognosis). Asfrom 32 weeks of gestation, the heart occupied its place on the left side of the chest and follow-up ultrasound confirmed a reduction in the pulmonary areaaffected by CAM. Normal Full-term delivery, with newborn weighing 3200 g, not requiring respiratory assistance. Normal post-natal chest x-ray.

Fig. 6: (a) Sagittal SS FSE T2, (b) Coronal SSFSE T2, (c) Axial SS FSE T2 and (d) CoronalT1-weighted dual echo gradient. CAM type IIin posterior segment of lower right lobe (whitearrow). GA: 28 weeks. Normal liver (arrowhe-ad) and colon's hepatic flexure (broken arrow).


sequestration does not have its own pleura and drai-nage is through pulmonary veins (40). They are rarelydiagnosed prenatally and are usually associated withtype II-CAM (hybrid lesions) (41). They have an exce-llent prognosis when isolated and over 50% resolve inutero (29). Large lesions may compress the esophagusand thoracic veins, and subsequently cause hydrops(an indication for fetal intervention and early delivery)(42). Prenatal treatment with thoracoamniotic shuntingis performed in cases of tension hydrothorax.

On MRI, pulmonary sequestration appears as asolid, hyperintense lesion on T2-weighted images,very similar to type III CAM. Identification of syste-mic blood supply helps in the diagnosis, mainly withbalanced sequences. MRI can detect small lesions andassociated anomalies.

Postnatally, most sequestrations are asymptomaticand may present with respiratory distress or cyanosis.Postnatal treatment consists of embolization of syste-mic blood supply or surgical resection, given the riskof infection, hemorrhage and questionable malig-nancy (mainly in hybrid lesions) (42).

Bronchogenic cyst

Bronchogenic cyst is the solitary cystic lesion mostcommonly found in the fetal chest. Most bronchoge-nic cysts appear as single lesions typically located inthe mediastinum, in the carinal region, and less fre-quently, in the hilar region (43). On MRI, it appears as awell-defined cyst, hyperintense on T2-weighted ima-ges when compared to the surrounding lung tissue(Fig. 9). In addition, the MRI can detect bronchial obs-truction due to mass effect of some cysts with hype-rintensity on T2-weighted images of the obstructedlobe (44). The role of MRI is limited to the cases of bron-chial obstruction, which will benefit from the EXIT-ECMO procedure with resection of the obstructivelesion, followed by reconstruction of the airway.

Bronchial obstruction by mucous plug

Obstruction by a mucous plug of a main or lobarbronchus produces an image similar to that of type-IIICAM or a sequestration with intrathoracic mass, hype-rintense on T2-weighted imaging, and which maycause mediastinal shift (Fig. 10). It may resolve sponta-neously in utero or by postnatal bronchoaspiration (45).


Fig. 7: (a) Coronal SS FSE T2. (b) Axial SSFSE T2. (c) Coronal FIESTA. (d) and (e) Ultrasounds. (1) Pulmonary sequestration presenting witha hyperintense solid component on T2, similar to type III-CAM. (2) Anomalous systemic vessel of the distal thoracic aorta. (3) Distal thoracicaorta. (4) Collapsed left lung parenchyma. (5) Right lung. GA: 28 weeks. Evolution: cesarean section at 38 weeks; Apgar scorer 8/10; 3100 g.Postnatal confirmation.



Fig. 9: (a) Sagittal FSE T2. (b) Sagittal FIESTA. (c) Axial SS FSE T2. (d) Coronal FIESTA. (e) Axial ultrasound and (f) sagittal ultrasound.Bronchogenic cyst in left lung (white arrow). GA: 22 weeks. Bichorial biamniotic twins.

Fig. 8: (a) and (b) Sagittal SS FSE T2. (c)Coronal SS FSE T2. (d) Axial SS FSE T2.Infradiaphragmatic sequestration (arrow) andsystemic artery of abdominal artery (arrowhe-ad). GA: 31.5 weeks.



Fig. 11: (a) and (b) Sagittal SS FSE T2. (c) Coronal SS FSE T2. (d) oblique slice SS FSE T2. (e) Axial SS FSE T2 (f) T1 gradient echo. Omphalocele:herniated liver (white arrow), stomach (curved arrow), bowel loops without meconium (broken arrow) and bowel loops with meconium (arrowhe-ad). GA: 20 weeks.

Fig. 10: (a) and (b) Coronal SS FSE T2. (c) and(d) Sagittal SS FSE T2. Affected LLL (whitearrow), healthy LUL (arrowhead) and healthyright lung (broken arrow) with normal x-rayat birth, corresponding to transient atelectasisdue to mucous plug. GA: 20.5 weeks.



Fig. 12: (a) 3D Ultrasound. (b) 2D Ultrasound(c) Sagittal SS FSE T2. (d) sagittal gradient-echo T1-weighted. Omphalocele (white arrow).Bowel loops with meconium (white arrowhead).GA: 28 weeks. Evolution: normal delivery andsubsequent surgical correction.

Other less common indications

Thoracic abnormalities less commonly assessed byMRI include: congenital airway obstruction (by extrin-sic factors or tracheal and bronchial stenotic or atresicmalformations), congenital lobar emphysema, pleuraleffusion, pericardial effusion, pericardial tumors (tera-toma), mediastinal tumors (teratoma, lymphangioma)and cardiac tumors (rhabdomyoma).

ABDOMINAL PATHOLOGY

Published studies on the usefulness of MRI inabdominal pathology are much less than those on tho-racic MRI. Even if most ultrasounds are diagnostic,they have limitations that create a need for an alterna-tive imaging method.

Anterior abdominal wall defects

The incidence of anterior abdominal wall defects is1 in 2000 live births (4). The commonest abdominal walldefects are gastroschisis and omphalocele and the lesscommon are the pentalogy of Cantrell (midline abdo-minal wall defect, anterior diaphragmatic hernia,diaphragmatic pericardial defect, lower sternal defectand cardiac abnormalities) and the cloacal and bladderexstrophy.

Omphalocele

An omphalocele is a midline supraumbilical abdo-minal wall defect with herniation of abdominal con-tent, covered by the peritoneum and amnion, withumbilical cord insertion in the apex of the omphaloce-le. The most commonly herniated organs are the liver,stomach and loops of the small bowel, which are easilyidentified on MRI. Omphalocele is associated withother malformations in 40 to 70% of cases and the inci-dence of chromosomal anomalies is 10 to 40%, inclu-ding trisomy 13, 14, 15, 18 and 21 (47).

The presence of liver in herniated organs has beenconsidered as the element that differentiates betweenlarge and small omphalocele. Large omphaloceleshave a high mortality rate, as several surgical procedu-res are required to obtain closure of the defect , withtheir main limitation being a small thoracic cavity,associated pulmonary hypoplasia and the need forprolonged mechanical ventilation (Fig. 11). On MRI,the presence of the liver in herniated organs is easilyidentified and the degree of pulmonary hypoplasiacan be established. Small omphaloceles (Fig. 12) showhigher association with chromosomal abnormalities (48).

Gastroschisis

Gastroschisis is a typically right-sided paraumbili-cal anterior abdominal wall defect (49). The loops of thesmall bowel are most frequently prolapsed and float in



Fig. 14: (a) and (b) Sagittal FIESTA. (c) Coronal FIESTA. (d) and (e) SS FSE T2-weighted urography images. (f) Coronal T1-weighted dual echogradient. Left renal agenesis. Hypertrophic right kidney (white arrow). Bladder (white arrowhead). Loops of small bowel (broken arrow) and colo-n’s splenic flexure (curved arrow) in the left renal fossa. GA: 32 weeks.

Fig. 13: (a) and (b) Coronal SS FSE T2. (c) and(d) Sagittal SS FSE T2. Single umbilicalartery (white arrow). Esophageal atresia withsmall-sized stomach (arrowhead) and smallesophageal pouch (broken arrow). Trachea(curved arrow). GA: 31.5 weeks.


the amniotic fluid without covering membrane.Extracorporeal colon may be present in gastroschisis,but not sigmoid or rectum. Prolapse of the liver lessfrequently occurs. A higher incidence is found inmothers using vasoactive substance (cocaine, nicotine,decongestants or aspirins) and in mothers youngerthan 25 years old. These defects are not generally asso-ciated with other malformations, although they mayaffect the gastrointestinal tract by 10-15% (atresia, ste-nosis, short bowel syndrome) probably due to ische-

mic damage by loop obstruction (50). They are associa-ted with oligohydramnios and intrauterine growthretardation (IUGR). When associated with polyhy-dramnios, bowel atresia or obstruction should be ruledout. MRI allows visualization in cases of oligohydram-nios or maternal obesity, or associated bowel compli-cations.

In 4-5% of cases, gastroschisis is associated withcardiac malformations (51). The incidence of chromoso-mal anomalies in gastroschisis is below 3% (52).


Fig. 15: (a) Coronal SS FSE T2. (b) Axial SS FSE T2. (c) Sagittal SS FSE T2. Multicystic right kidney (arrow). Normal left kidney (arrowhead).GA: 20 weeks.

Fig. 16: Bichorial biamniotic twin pregnancy. Cloacal malformation. (a) Ultrasound at 15 weeks of gestation: rectal-sigmoid dilation (white arrow)and fecal impaction (white arrowhead) in one twin, without ascites. (b) Ultrasound at 20 weeks of gestation: cystic structure with incomplete sep-tum (broken arrow), anterior to rectosigmoid and posterior to the bladder (black arrow), with ambiguous genitalia. MRI was performed at 26.5weeks of gestation. (c) Sagittal SS FSE T2 and (d) Sagittal SS FSE T2 (URO-MRI). Ascites (black arrowhead) of the twin in longitudinal posi-tion and left breech presentation. Cystic structure (broken arrow)anterior to the rectum-sigmoid. (e) and (f) Coronal FIESTA. Ascites (black arro-whead) and cystic structure with incomplete septum (broken arrow) with content inside (curved arrow), suggesting detritus from fistula of the rec-tosigmoid (white arrow). Bladder cannot be identified. G SS FSE T2 (URO-RM). Grade III/IV hydronephrosis on the right side (1) grade II/IVhydronephrosis on the left side (2), suggesting urinary ascites. Postnatal follow-up by x-ray: retrograde filling of contrast material through singleperineal opening (3). Filling of bladder (4), vagina and partial septate uterus (5) containing hydrometrocolpos and gas because of rectosigmoid fis-tula. The rectosigmoid is not filled with contrast (6).



Fig. 17: Cystic lymphangioma (a) and (b) Axial SS FSE T2. (c) Sagittal SS FSE T2. (d) Coronal FIESTA. Multiseptated cystic lymphangioma ofthe mesenterium, greater omentum and ileocecal region, hyperintense on T2-weighted images (white arrow). The lesion is independent of the rightkidney (arrowhead), displaces the small bowel loops to the left side of the abdomen (curved arrow) indenting the bladder dome (broken arrow). (3)3D LAVA. The lymphangioma appears hypointense on T1-weighted images (white arrow) with no evidence of bleeding and indenting the bladderdome (broken arrow). (f) 3D LAVA. Coronal MIP reconstruction. Cranial displacement of the transverse colon (black arrow). GA: 33.3 weeks.

GASTROINTESTINAL ABNORMALITIES

Fetal scan of the gastrointestinal tract is based onthe presence of “natural” contrast media: swallowedamniotic fluid passed to the intestines and meconium.Swallowing of amniotic fluid begins by 9-10 gestatio-nal weeks (53); however, except for the stomach, it is notuntil 25 gestational weeks that significant amount offluid enters the fetal intestines to serve as a naturalcontrast medium. The full-term fetus swallows asmuch as 750 ml/day. Meconium starts to accumulatein the rectum by 18-20 gestational weeks, with retro-grade filling of the colon and distal ileal loops.

Most abnormalities are diagnosed by ultrasoundand do not require a complementary diagnostic method.

The main indications for MRI in gastrointestinalassessment are: identifying the site of bowel obstruc-tion (bowel atresias, meconium ileus and bowel volvu-lus) and ruling out bowel ischemia (wall thickening,meconium peritonitis) and malrotation.

Esophageal atresia

The most common is type A with proximal atresiaand distal tracheoesophageal fistula. Diagnosis is esta-blished by the presence of polyhydramnios, small sto-

mach, proximal esophageal pouch and IUGR in the2nd or 3rd trimester (34) (Fig. 13). The tracheoesophage-al fistula cannot be detected by MRI. It is associatedwith trisomy 18 and, in the absence of fistula, it is morecommon in trisomy 21.

Duodenal atresia or stenosis

Duodenal atresia or stenosis is diagnosed bymeans of the double bubble sign of the stomach andduodenum (hypointense on T1-weighted images andhyperintense on T2-weighted sequences) (55), whichincludes duodenal stenosis, annular pancreas, Laddbands and volvulus. Duodenal atresia is associatedwith other abnormalities and trisomy 21 (56)-

Small bowel atresia or stenosis

Small bowel atresia is seen as dilated bowel loopsproximal to the obstructed segment. MRI providesadditional information since in the case of jejunal ste-nosis or atresia, dilated loops are hypointense on T1-weighted images and hyperintense on T2-weightedimages (with triple bubble sign and polyhydramnios,if proximal jejunum is affected) while in ileal atresia or



Fig. 18: Retroperitoneal teratoma. (a) and (b) Axial SS FSE T2. (c) and (d) Coronal SS FSE T2. (e) Sagittal Fiesta. (f) Sagittal T1-weighted echogradient. Cystic mass on right adrenal location, with solid poles (white arrow), crossing the midline (arrowhead) anterior to the aorta. The massinferiorly displaces the right kidney with horizontalization of the kidney (curved arrow). GA: 35.5 weeks.

stenosis, dilated loops resemble a “string of sausages”with meconium, being hyperintense on T1-weightedimages and iso-hypointense on T2-weighted images(57). Distal atresias have a higher risk of perforation andmeconium peritonitis.

Meconium peritonitis

Meconium peritonitis is a chemical peritonitissecondary to the perforation of a bowel loop, diagno-sed on US with the finding of peritoneal calcification,ascites and pseudocysts (54). MRI cannot identify calcifi-cations but allows easy recognition of dilated loops,ascites, polyhydramnios and cystic masses (meconiumpseudocysts). Pseudocysts may contain internal septa-tions with a variable T1 signal and a high T2 signal (58),hyperintense on T1-weighted images and intermedia-te on T2-weighted images (59) or hyperintense on T1-and very low on T2-weighted images (60).

Colon malrotationsMalrotations can be diagnosed on MRI as from 25

weeks of gestation. MRI shows the abnormal positionof the colon, using T1-weighted sequences, givenmeconium content (55).

Megacystis-Microcolon–Intestinal HypoperistalsisSyndrome

Enlarged bladder (the most typical finding) iseasily diagnosed on ultrasound and MRI. On MRI, thisfinding can be visualized as from 25 weeks of gestationgiven the very small amounts of meconium present inthe rectum. At the end of gestation, more meconiumaccumulates and the microcolon can be seen (55).

Large bowel atresia

Large bowel atresia mainly affects the rectum.Atresia of the transverse colon produces dilation of theproximal colon, small amount of distal meconium anddilation of small bowel loops with absence of peristal-sis. Cecal atresia causes dilation of the cecum andileum with abundant meconium (61).

Hirschsprung disease

In Hirschsprung's disease, there is rectal dilationwith hypointense inverted signal on T1-weighted ima-ges and intermediate signal on T2-weighted images (62).


Anal atresia

Small and isolated forms of anal atresia may goundetected by MRI. V-shaped or U-shaped loops inthe pelvis suggest a diagnosis of anal atresia. They arefrequently associated with urinary tract fistula produ-cing enteroliths (which are bettered identified on ultra-sound) (63) or they may be part of the VACTERL syndro-me ((vertebral anomalies, anal atresia, cardiac anoma-lies, tracheoesophageal fistula, renal and limb defect).

GENITOURINARY ABNORMALITIES

Fetal urine is the main source of amniotic fluid. Asfrom 10 weeks’ gestation, fetal kidneys produce urineand during the second half of pregnancy, they produ-ce 90% of amniotic fluid.

MRI is indicated only when ultrasound findings areinconclusive, especially in the cases of oligohydram-nios or anhydramnios. 2D and 3D T2-weighted sequen-ces with long repetition time (RT) are useful to obtainurography images of the excretory system withoutintravenous contrast (which is contraindicated).

Diffusion-weighted sequence would be useful incases of suspected renal infarction due to venousthrombosis with a decrease in the apparent diffusioncoefficient (ADC) and in the twin-twin transfusionsyndrome, where the ADC of the donor twin is higherthan that of the recipient twin and is related to theseverity of the syndrome. Diffusion-weighted ima-ging helps in the diagnosis of (unilateral or bilateral)renal agenesis because this technique is very sensitivein detection of the renal parenchyma (64, 65).

Hydronephrosis

Hydronephrosis is clearly visualized on T2-weigh-ted images. In the coronal plane, urography imagescan be obtained, with visualization of the whole ure-teral course (66).

Pyeloureteral junction stenosis

The pyeloureteral junction stenosis is the most fre-quent cause of hydronephrosis detected prenatally (67)

and it may progress to a displastic kidney with multi-ple cortical and medullary cysts.

Duplicated renal collecting system

A duplicated renal collecting system is the mostcommon anomaly (68). MRI can be helpful in the diag-nosis of complete or incomplete duplex system, andectopic drain of an ureterocele associated with theupper ureter.

Bilateral renal agenesis

MRI allows diagnosis of bilateral renal agenesis, assevere oligohydramnios or anhydramnios impairsassessment by US. It is associated with congenitalheart disease and Potter's syndrome due to oligohy-dramnios (typical facies, joint contractures and pul-monary hypoplasia) (69).

Unilateral renal agenesis

Unilateral renal agenesis (Fig. 14) generally occursin isolation, and has a normal life expectancy,although it may be occasionally associated with VAC-TERL syndrome. When a kidney is not located withinthe renal fossa, MRI helps in identification of the ecto-pic kidney location.

Autosomal polycystic kidney disease

Autosomal recessive polycystic kidney disease ischaracterized by large kidneys with high uniformintensity on T2-weighted images and loss of cortico-medullary differentiation; the pyelocaliceal system isnot identified (70).

Multicystic dysplastic kidney

Multicystic dysplastic kidneys (Fig. 15) are enlar-ged, with multiple cysts of different size peripherallyand centrally located, with little renal parenchyma (71).These cysts demonstrate high signal intensity on T2-weighted sequences and are separated from the pye-localiceal system.

Bladder exstrophy

Bladder exstrophy is a rare malformation in whichthe anterior wall of the bladder is absent, and the pos-terior wall is exposed externally. MRI identifies anextruded solid mass below the umbilical cord inser-tion , with normal kidneys and amniotic fluid (72).

Cloacal malformation

Cloacal malformation is a rare cause of obstructiveuropathy secondary to failure of the division of theprimitive cloaca, with communication between thegastrointestinal, urinary, and genital structures, resul-ting in a single perineal opening. Cloacal malforma-tion is more common in women, with bilateral hydro-nephrosis, cystic lesion in the pelvis and difficulty invisualizing the bladder because of its small size (Fig.16). It is associated with meconium calcification in the




Fig. 20: Portosystemic shunt with aneurysm or venous lake in 30-gestational-week-old fetus. (a), (b), (c), (d) and (e) MRI. Axial FIESTA; (f) SagittalFIESTA. Umbilical cord (curved arrow). Absence of venous conduit, with umbilical vein (black arrow) draining into the portal vein (arrowhead) atthe level of the hepatic hilum. Venous lake or aneurysm (white arrow) in segment VIII. Anterior drainage vein (1). Posterior drainage vein (2). Vesselcollecting blood from (1) and (2) and draining into the inferior vena cava (3). Inferior vena cava (broken arrow). Left hepatic vein (black arrowhead).

Fig. 19: (a) Coronal FIESTA (b), (c), (d), (e) and (f) Axial FIESTA. (1) Supradiaphragmatic inferior vena cava; (2) Middle hepatic vein, (3) lefthepatic vein; (4) right atrium; (5) descending thoracic aorta; (6) azygos vein; (7)abdominal aorta; (8) hemiazygos vein; (9) right hepatic vein; (10)left ascending lumbar vein. Agenesis of inferior vena cava secondarty to thrombosis, with collateral flow through paravertebral veins, azygos andhemiazygos ascending lumbar veins. Bilateral adrenal hemorrhagic pseudocysts. Kidneys with cortical thickening (white arrows), mainly on theleft kidney. (g) Sagittal SS FSE T2. Left adrenal hemorrhagic pseudocyst and high signal intensity in the upper pole of kidney, suggesting renalinfarction (broken arrow). (h) Diffusion-weighted image. High intensity signal of left kidney suggesting probably venous infarction (white arro-whead). GA: 36 weeks.


urinary tract and colon, which are better identified onultrasound (72, 74). There is a minor variant: the urogeni-tal sinus, with communication between the vaginaand the urinary tract (which normally occurs duringembryological development). Such communicationmay occur at any point from the urethral meatus tothe bladder, but the majority occur within the mid todistal portion of the urethra. The two structures joinand exit on the perineum as a single common uroge-nital sinus channel (75).

Prune-Belly or Eagle-Barrett Syndrome

The Prune-Belly or Eagle-Barrett Syndrome is arare congenital malformation with severe hydroneph-rosis, abdominal muscle deficiency and chryptorchi-dism. MRI identifies hydronephrosis, bilateral urete-ral dilatation and dilation of the entire urethra, unlikeposterior valves, which cause proximal urethral dila-tation. Genitalia are absent and it is associated witholigohydramnios (76).

ABDOMINAL MASSES

Most abdominal masses are benign cystic lesions:Intestinal duplication cyst: unilocular cyst, with

double-layered wall of muscle and mucous membra-ne. The most common location is in the distal ileum.

Mesenteric cyst: considered as a lymphatic malfor-mation. It may be unilocular or most commonly multi-locular with multiple septa (Fig. 17). It may occasio-nally extend into the retroperitoneum and lower limbs.

Ovarian cyst: this is the most common femaleabdominal mass in the third trimester. Ovarian liga-ments are lax and the ovarian cyst may be found inany location. It may be simple or complicated, withtorsion and bleeding.

Urachal cyst: unilocular cyst that occurs in themidline between the bladder and the umbilical cordinsertion.

Choledocal cyst: unilocular cyst that occurs in theright upper quadrant. Bile ducts may be seen enteringinto the cyst.

TUMORS

MRI can detect, localize and characterize benigncystic lesions, differentiating them from bowel loops (77, 78).

The experience with MRI in the diagnosis of conge-nital hepatic masses is very limited. Most are large andsolid masses (hemangioendothelioma, hepatoblasto-ma or metastatic neuroblastoma) , with cystic lesions(mesenchymal hamartoma) being less common (79).

Mesoblastic nephroma is the most common renalsolid mass. It is a benign tumor with excellent progno-sis associated in 70% of cases with polyhydramnios (80).

MRI can better delimitate its organ-dependence. Itappears as a solid mass of uniform, slightly hyperin-tense signal on T2-weighted images.

Neuroblastoma is the most common malignanttumor in the newborn (81). Most neuroblastomas arisefrom the adrenal medulla and they can be solid, cystic orsolid and cystic adrenal masses(82). Liver metastases arecommon (82). Differential diagnosis with adrenal hemor-rhage should be established (MRI identifies hemorrhagein different stages) (83), infradiaphragmatic pulmonarysequestration (MRI can show systemic blood supply) (84)

and retroperitoneal teratomas (85) (Fig. 18).

VASCULAR PATHOLOGY IMAGING

The use of intravenous contrast (gadolinium) isnot accepted. Gadolinium chelates cross the placenta(86) and there is potential risk of gadolinium-inducednephrotoxicity (nephrogenic systemic fibrosis) (87).

Balanced sequences (FIESTA) are useful in asses-sing thoracic and abdominal vascular anatomywithout contrast (88), mainly in cases of intra- or extra-lobar sequestration, developmental abnormalities ofthe inferior vena cava (Fig. 19) or vascular malforma-tions such as hepatic portosystemic shunts (Fig. 20).

CONCLUSIONS

MRI plays an important role as complementarymethod to ultrasound due to its multiplanar capabi-lity and tissue differentiation. Its main indication isthe assessment of diaphragmatic hernia, where MRIprovides diagnostic information, establishes a prog-nosis and helps in planning delivery and postnatalsurgery. In gastrointestinal pathology, MRI is useful inthe assessment of bowel obstruction, perforation andmalrotation. In genitourinary imaging, MRI does nothave the limitations of ultrasound (oligohydramniosor maternal obesity) and it is used in the assessment ofrenal agenesis, obstructive pathology and cystic kid-ney disease. Furthermore, it allows characterization ofcongenital cystic lesions. With balanced sequences,MRI angiographies can be performed without intra-venous contrast; this is useful in the assessment ofcongenital vascular pathology of large vessels andpulmonary sequestration.

References

1. Shinmoto H, Kashima K, Yuasa Y, et al. MR imaging of non-CNS fetal abnormalities: a pictorial essay. RadioGraphics2000; 20:1227-43.

2. Cannie M, Jani J, De Keyzer F, Roebben I, Dymarkowski S,Deprest J. Diffusion-weighted MRI in lungs of normal fetu-ses and those with congenital diaphragmatic hernia.Ultrasound Obstet Gynecol 2009; 34:678-86.



3. Chaumoitre K, Colavolpe N, Shojai R, Sarran A, D’ Ercole C,Panuel M. Diffusion-weighted magnetic resonance imagingwith apparent diffusion coefficient (ADC) determination innormal and pathological fetal kidneys. Ultrasound ObstetGynecol 2007; 29:22-31.

4. Levine D, Barnewolt CE, Mehta TS, Trop I, Estroff J, Wong G.Fetal thoracic abnormalities: MR imaging. Radiology 2003;228:379-88.

5. Butler N, Claireaux AE Congenital diaphragmatic hernia asa cause of perinatal mortality. Lancet 1962; 1:659-63.

6. Torfs CP, Curry CJ, Bateson TF, Honoré LH. A population-based study of congenital diaphragmatic hernia. Teratology1992; 46:555-65.

7. Witters I, Legius E, Moerman P, et al. Associated malforma-tions and chromosomal anomalies in 42 cases of prenatallydiagnosed diaphragmatic hernia. Am J Med Genet 2001;103:278-82.

8. Skari H, Bjornland K, Haugen G, Egeland T, Emblem R.Congenital diaphragmatic hernia: a meta-analysis of marta-lity factors. J Pediatr Surg 2000; 35:1187-97.

9. Jani J, Peralta CFA, Van Schoubroeck D, Deprest J,Nicolaides KH. Relation between lung-to-head ratio andlung volume in normal fetuses and fetuses with diaphrag-matic hernia. Ultrasound Obstet Gynecol 2006; 27:545-50.

10. Jani J, Cannie M, Peralta CFA, Deprest J, Nicolaides KH,Dymarkowski S. Lung volumes in fetuses with congenitaldiaphragmatic hernia: comparison of 3D US and MRImaging assessments. Radiology 2007; 244:575-82.

11. Rypens F, Metens T, Rocourt N, et al. Fetal lung volume: esti-mation at MR imaging-initial results. Radiology 2001;219:236-41.

12. Coakley FV, Lopoo JB, Lu Y, et al. Normal and hypoplasticfetal lungs: volumetric assessment with prenatal single-shotrapid acquisition with relaxation enhancement MR imaging.Radiology 2000; 216:107-11.

13. Cannie M, Jani J, Van Kerkhove F, et al. Fetal body volume atMR imaging to quantify total fetal lung volume normal ran-ges. Radiology 2008; 247:197–203.

14. Paek BW, Coakley FV, Lu Y, et al. Congenital diaphragmatichernia: prenatal evaluation with MR lung volumetry-preli-minary experience. Radiology 2001; 220:63-7.

15. Kilian AK, Schaible T, Hofmann V, et al. Congenital diaphrag-matic hernia: predictive value of MRI relative lung-to-headratio compared with MRI fetal lung volume and sonographiclung-to-head ratio. AJR Am J Roentgenol 2009; 192:153-8.

16. Osada H, Kaku K, Masuda K, Iitsuka Y, Seki K, Sekiya S.Quantitative and qualitative evaluations of fetal lung withMR imaging. Radiology 2004; 231:887-92.

17. Balassy C, Kasprian G, Brugger PC, et al. MRI investigationof normal fetal lung maturation using signal intensities ondifferent imaging sequences. Eur Radiol 2007; 17:835-42.

18. Sedin G, Bogner P, Berényi E, Repa I, Nyúl Z, Sulyok E. Lungwater and proton magnetic resonance relaxation in pretermand term rabbit pups: their relation to tissue hyaluronan.Pediatr Res 2000; 48:554-9.

19. Moore RJ, Strachan B, Tyler DJ, Baker PN, Gowland PA. Invivo diffusion measurements as an indication of fetal lungmaturation using echo planar imaging at 0.5T. Magn ResonMed 2001; 45:247-53.

20. Manganaro L, Perrone A, Sassi S, et al. Diffusion-weightedMR imaging and apparent diffusion coefficient of the normalfetal lung: preliminary experience. Prenat Diagn 2008;28:745-8.

21. Cannie M, Jani J, De Keyzer F, Roebben I, Dymarkowski S,Deprest J. Diffusion-weighted MRI in lungs of normal fetu-

ses and those with congenital diaphragmatic hernia.Ultrasound Obstet Gynecol. 2009; 34:678-86.

22. Fenton BW, Lin CS, Seydel F, Macedonia C. Lecithin can bedetected by volume-selected proton MR spectroscopy usinga 1.5 T whole body scanner: a potentially non-invasivemethod for the prenatal assessment of fetal lung maturity.Prenat Diagn 1998; 18:1263-6.

23. Fenton BW, Lin CS, Ascher S, Macedonia C. Magnetic reso-nance spectroscopy to detect lecithin in amniotic fluid andfetal lung. Obstet Gynecol 2000; 95:457-60.

24. Cannie MM, Jani JC, De Keyzer F, Allegaert K, DymarkowskiS, Deprest J. Evidence and patterns in lung response afterfetal tracheal occlusion: clinical controlled study. Radiology2009; 252:526-33.

25. Jani JC, Benachi A, Nicolaides KH, et al. Prenatal predictionof neonatal morbidity in survivors with congenital diaph-ragmatic hernia: a multicenter study. Ultrasound ObstetGynecol 2009; 33:64-9.

26. Achiron R, Hegesh J, Yagel S. Fetal lung lesions: a spectrumof disease. New classification based on pathogenesis, two-dimensional and color Doppler ultrasound. UltrasoundObstet Gynecol 2004; 24:107-14.

27. Achiron R, Zalel Y, Lipitz S, et al. Fetal lung dysplasia: clini-cal outcome based on a new classification system.Ultrasound Obstet Gynecol 24:127-33.

28. Stocker JT, Madewell JE, Drake RM. Congenital cystic ade-nomatoid malformation of the lung. Classification and mor-phologic spectrum. Hum Pathol 1977; 8:155-71.

29. Cavoretto P, Molina F, Poggi S, Davenport M, NicolaidesKH. Prenatal diagnosis and outcome of echogenic fetal lunglesions. Ultrasound Obstet Gynecol 2008; 32:769-83.

30. Quinn TM, Hubbard AM, Adzick NS. Prenatal magneticresonance imaging enhances fetal diagnosis. J Pediatr Surg1998, 33:553-8.

31. Liu YP, Chen CP, Shih SL, Chen YF, Yang FS, Chen SC. Fetalcystic lung lesions: evaluation with magnetic resonance ima-ging. Pediatr Pulmonol 2010; 45:592-600.

32. Rosado-de-Christenson ML, Stocker JT Congenital cysticadenomatoid malformation. RadioGraphics 1991; 11:865-86.

33. Grethel EJ, Wagner AJ, Clifton MS, et al. Fetal interventionfor mass lesions and hydrops improves outcome: a15-yearexperience. J Pediatr Surg 2007; 42:117-23.

35. Vu L, Tsao KJ, Lee H, et al. Characteristics of congenitalcystic adenomatoid malformations associated with nonim-mune hydrops and outcome. J Pediatr Surg 2007; 42:1351-6.

36. Laberge JM, Puligandla P, Flageole H. Asymptomatic conge-nital lung malformations. Semin Pediatr Surg 2005; 14:16-33.

37. Savic B, Birtel FJ, Tholen W, Funke HD, Knoche R. Lungsequestration: report of seven cases and review of 540published cases. Thorax 1979; 34:96–101.

38. Laje P, Martinez-Ferro M, Grisoni E, Dudgeon D.Intraabdominal pulmonary sequestration. A case series andreview of the literature. J Pediatr Surg 2006; 41:1309-12.

39. Laurin S, Hägerstrand I. Intralobar bronchopulmonarysequestration in the newborn: a congenital malformation.Pediatr Radiol 1999; 29:174-8.

40. Winters WD, Effmann EL. Congenital masses of the lung:prenatal and postnatal imaging evaluation. J Thorac Imaging2001; 16:196–206.

41. Zeidan S, Hery G, Lacroix F, et al. Intralobar sequestrationassociated with cystic adenomatoid malformation: diagnos-tic and thoracoscopic pitfalls. Surg Endosc 2009; 23:1750-3

42. Azizkhan RG, Crombleholme TM. Congenital cystic lungdisease: contemporary antenatal and postnatal manage-ment. Pediatr Surg Int 2008; 24:643-57.



43. Takeda S, Miyoshi S, Minami M, Ohta M, Masaoka A,Matsuda H. Clinical spectrum of mediastinal cysts. Chest2003; 124:125-32.

44. Levine D, Jennings R, Barnewolt C, Mehta T, Wilson J, WongG. Progressive fetal bronchial obstruction caused by abron-chogenic cyst diagnosed using prenatal MR imaging. AJRAm J Roentgenol 2001; 176:49–52.

45. Meizner I, Rosenak D. The vanishing fetal intrathoracicmass: consider an obstructing mucous plug. UtrasoundObstet Gynecol 1995; 5:275-7.

46. Nyberg DA, Mack LA. Abdominal wall defects. En: NybergDA, Mahony BS, Pretorius DH, eds. Diagnostic ultrasoundof fetal anomalies. St. Louis: Mosby; 1990: 395.

47. Ledbetter DJ. Gastroschisis and omphalocele. Surg ClinNorth Am 2006; 86:249-60, vii.

48. Nyberg DA, Fitzsimmons J, Mack LA, et al. Chromosomalabnormalities in fetuses with omphalocele. Significance ofomphalocele contents. J Ultrasound Med 1989; 8: 299-308.

49. De Vries PA. The pathogenesis of gastroschisis and ompha-locele. J Pediatr Surg 1980; 15:245-51.

50. Louw JH, Barnard CN. Congenital intestinal atresia.Observations on its origin. Lancet 1955; 269:1065-7.

51. Kunz LH, Gilbert WM, Towner DR. Increased incidence ofcardiac anomalies in pregnancies complicated by gastroschi-sis. Am J Obstet Gynecol 2005; 193:1248-52.

52. Eggink BH, Richardson CJ, Malloy MH, Angel CA. Outcomeof gastroschisis: a 20-year case review of infants with gas-troschisis born in Galveston, Texas. J Pediatr Surg 2006;41:1103-8.

53. Dumont RC, Rudolph CD. Development of gastrointestinalmotility in the infant and child. Gastroenterol Clin North Am1994; 23:655-71.

54. Nyberg DA, Neilsen IR. Abdomen and gastrointestinal tract.En: Nyberg NA, McGahan JP, Pretorius DH, Pilu G, eds.Diagnostic imaging of fetal anomalies. Philadelphia:Lippincott Williams & Wilkins; 2003:551-602.

55. Brugger PC. MRI of the fetal abdomen. En: Prayer D, ed.Fetal MRI. Verlag Berlin Heidelberg: Springer; 2011: 377-98.

56. Tongsong T, Wanapirak C, Sirichotiyakul S, Sirivatanapa P.Prenatal sonographic markers of trisomy 21. J Med AssocThai 2001; 84:274-80.

57. Carcopino X, Chaumoitre K, Shojai R, Panuel M, Boubli L,D’Ercole C. Use of fetal magnetic resonance imaging in dif-ferentiating ileal atresia from meconium ileus. UltrasoundObstet Gynecol 2006; 28:976-7.

58. Simonovsky V, Lisy J. Meconium pseudocyst secondary toileal atresia complicated by volvulus: antenatal MR demons-tration. Pediatr Radiol 2007; 37:305-9.

59. Garel C, Dreux S, Philippe-Chomette P, Vuillard E, Oury JF,Muller F. Contribution of fetal magnetic resonance imagingand amniotic fluid digestive enzyme assays to the evalua-tion of gastrointestinal tract abnormalities. UltrasoundObstet Gynecol 2006; 28:282-91.

60. Carcopino X, Chaumoitre K, Shojai R, et al. Foetal magneticresonance imaging and echogenic bowel. Prenat Diagn 2007;27:272-8.

61. Hill BJ, Joe BN, Qayyum A, Yeh BM, Goldstein R, CoakleyFV. Supplemental value of MRI in fetal abdominal diseasedetected on prenatal sonography: preliminary experience.AJR Am J Roentgenol 2005; 184:993-8.

62. Ohgiya Y, Gokan T, Hamamizu K, Moritani T, Kushihashi T,Munechika H. Fast MRI in obstetric diagnoses. J ComputAssist Tomogr 2001; 25:190–20.

63. Sepulveda W, Romero R, Qureshi F, Greb AE, Cotton DB.Prenatal diagnosis of enterolithiasis: a sign of fetal large

bowel obstruction. J Ultrasound Med 1994; 13:581-5.64. Chaumoitre K, Colavolpe N, Shojai R, Sarran A, D’Ercole C,

Panuel M. Diffusion-weighted magnetic resonance imagingwith apparent diffusion coefficient (ADC) determination innormal and pathological fetal kidneys. Ultrasound ObstetGynecol 2007; 29: 22–31.

65. Witzani L, Brugger PC, Hörmann M, Kasprian G, Csapone-Balassy C, Prayer D. Normal renal development investigatedwith fetal MRI. Eur J Radiol 2006; 57:294–302.

66. Fradin JM, Regan F, Rodriquez R, Moore R. Hydronephrosisin pregnancy: simultaneous depiction of fetal and maternalhydronephrosis by magnetic resonance urography. Urology1999; 53:825-7.

67. Guys JM, Borella F, Monfort G. Ureteropelvic junction obs-tructions: prenatal diagnosis and neonatal surgery in 47cases. J Pediatr Surg 1988; 23:156-8.

68. Jeffrey RB, Laing FC, Wing VW, Hoddick W. Sonography ofthe fetal duplex kidney. Radiology 1984; 153:123-4.

69. Potter EL. Bilateral absence of ureters and kidneys: a reportof 50 cases. Obstet Gynecol 1965; 25:3-12.

70. Mine K, Suzuki S, Watanabe S, et al. Prenatal diagnosis ofautosomal recessive polycystic kidney disease. A case report.Nihon Ika Daigaku Zasshi 1999; 66:188-90.

71. Ohgiya Y, Gokan T, Hamamizu K, Moritani T, Kushihashi T,Munechika H. Fast MRI in obstetric diagnoses. J ComputAssist Tomogr 2001; 25:190-200.

72. Lee EH, Shim JY. New sonographic finding for the prenataldiagnosis of bladder exstrophy: a case report. UltrasoundObstet Gynecol 2003; 21:498-500.

73. Warne S, Chitty LS, Wilcox DT. Prenatal diagnosis of cloacalanomalies. BJU Int 2002; 89:78-81.

74. Gupta P, Kumar S, Sharma R, Gadodia A. Case report:Antenatal MRI diagnosis of cloacal dysgenesis syndrome.Indian J Radiol Imaging 2010; 20:143-6.

75. Campbell- Walsh. Urología. Tomo 4. Buenos Aires: EditorialMédica Panamericana; 2009: 3846-51.

76. Caire JT, Ramus RM, Magee KP, Fullington BK, Ewalt Dh,Twickler DM. MRI of fetal genitourinary anomalies. AJR AmJ Roentgenol 2003; 181:1381-5.

77. Breysem L, Bosmans H, Dymarkowski S, et al. The value offast MR imaging as an adjunct to ultrasound in prenataldiagnosis. Eur Radiol 2003; 13:1538-48.

78. Shinmoto H, Kuribayashi S. MRI of fetal abdominal abnor-malities. Abdom Imaging 2003; 28:877-86.

79. Brunelle F, Chaumont P. Hepatic tumors in children: ultraso-nic differentiation of malignant from benign lesions.Radiology 1984; 150:695-9.

80. Leclair MD, El-Ghoneimi A, Audry G, Ravasse P, MoscoviciJ, Heloury Y. French Pediatric Urology Study Group. Theoutcome of prenatally diagnosed renal tumors. J Urol 2005;173:186-9.

81. Kesrouani A, Duchatel F, Seilanian M, Muray JM. Prenataldiagnosis of adrenal neuroblastoma by ultrasound: a reportof two cases and review of the literature. Ultrasound ObstetGynecol 1999; 13:446-9.

82. Toma P, Lucigrai G, Marzoli A, Lituania M. Prenatal diagno-sis of metastatic adrenal neuroblastoma with sonographyand MR imaging. AJR Am J Roentgenol 1994; 162:1183-4.

83. Trop I, Levine D. Hemorrhage during pregnancy: sono-graphy and MR imaging. AJR Am J Roentgenol 2001;176:607-15.

84. Plattner V, Haustein B, Llanas B, Allos N, Vergnes P, HélouryY. Extra-lobar pulmonary sequestration with prenatal diag-nosis. A report of 5 cases and review of the literature. Eur JPediatr Surg 1995; 5:235-7.



85. Woodward PJ, Sohaey R, Kennedy A, Koeller KK. From thearchives of the AFIP: a comprehensive review of fetal tumorswith pathologic correlation. RadioGraphics 2005; 25:215-42.

86. Webb JA, Thomsen HS, Morcos SK. The use of iodinated andgadolinium contrast media during pregnancy and lactation.Eur Radiol 2005; 15:1234-40.

87. Grobner T, Prischl FC. Gadolinium and nephrogenic systemic

fibrosis. Kidney Int 2007; 72:260-4.88. Prayer D, Brugger PC. Investigation of normal organ deve-

lopment with fetal MRI. Eur Radiol 2007; 17: 2458-71.

AcknowledgementsWe thank Sergio García Fauró, radiologic technologist.


obstetric revision article internacional colaboration ... · obstetric revision article...

Documents